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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The intestinal mucosa is an important portal of entry of HIV, and HIV-infected mononuclear cells are found in the intestinal lamina propria of 30 to 50% of HIV-infected patients even at early stages of the disease. HIV infection of epithelial cells has not consistently been detected and is still controversial. Intestinal T cells are phenotypically and functionally distinct from circulating T cells, especially in their state of activation and differentiation, which both affect the replication and cytopathicity of HIV. An increase in CD8+ cells and variable decreases in CD4+ cells have been found in the intestinal lamina propria by immunohistologic studies, resulting in a decreased CD4 to CD8 ratio; in addition, CD25 expression is reduced. Changes in intraepithelial lymphocytes are unclear. B-cell differentiation seems to be disturbed because IgA plasma cells and IgA2 secretion are reduced. Depletion or functional impairment of activated mucosal lamina propria lymphocytes by HIV infection could explain the breakdown of the mucosal immune barrier leading to opportunistic diseases; in addition, due to the interrelationship between mucosal immune system and epithelium, these changes might be responsible for the partial bowel atrophy and maturational defects in enterocytes of HIV-infected patients.
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PMID:Enteric immunologic abnormalities in human immunodeficiency virus infection. 163 19

During the period February 1987-June 1988, the authors examined 542 stool samples of 271 HIV-positive patients both with and without fullblown AIDS. 100 patients with either acute or chronic diarrhea and 180 without diarrhea were studied. The stool samples were examined for the presence of Cryptosporidium sp., other protozoa, helminths, and pathogenic enterobacteria. A prevalence of 14.3% of Cryptosporidium sp. in patients with fullblown AIDS and diarrhea was found. No Cryptosporidium sp. was seen among asymptomatic patients. The occurrence of diarrhea was significantly associated with a CD4/CD8 ratio lower than 0.4, with the finding of Cryptosporidium sp. in the stools, being a CDC group IV, and with a positive stool culture for pathogenic enterobacteria. The diarrhea caused by Cryptosporidium sp. could not be distinguished on clinical grounds from diarrhea caused by other etiologic agents. (author's modified) (summaries in ENG, POR
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PMID:[Prevalence of cryptosporidiosis in diarrheic syndrome in HIV positive patients]. 165 76

Cellular immunity is known to play a critical role in regulating Epstein-Barr virus (EBV) in the state of latent infection. Activity of EBV-specific cellular immunity decreases as the clinical stages of human immunodeficiency virus (HIV) infection progress, and many complications are induced by reactivated EBV in the late stages of HIV infection. However, in asymptomatic HIV carriers, some show the reduced activity of cellular immunity against EBV, while others still show normal range of the activity even in the presence of abnormality in other immunological parameters. In order to assess early immunological abnormality against EBV in these patients, asymptomatic HIV carriers with normal range of EBV-specific cellular immunity were studied in comparison with that in EBV seropositive healthy controls. 1. All of 4 asymptomatic HIV carriers showed normal range of EBV-specific cellular immunity as seen in healthy controls. 2. Asymptomatic HIV carriers had significantly elevated serum antibody titers to EBV-specific nuclear antigen (EBNA)2, viral capsid antigen(VCA), early antigen(EA), indicative of serological reactivation of EBV. 3. The number and percentage of peripheral CD4 positive lymphocytes, CD4/CD8 ratios were markedly decreased in asymptomatic HIV carriers. 4. In the presence of immunosuppressive agents, 4-deoxy phorbol ester(4-DPE), drastic decrease of EBV-specific cellular immunity was observed in asymptomatic HIV carriers at the concentration which did not affect that of healthy controls. 5. Reduced activity of EBV-specific cellular immunity induced by 4-DPE had no relation with surface marker expression on cytotoxic T cells which serve as cell-to-cell adhesion molecules. Based on these results, it is suggested that there is latent dysfunction of EBV-specific cellular immunity in asymptomatic HIV carriers, who seems to show normal range of immunity in usual assays.
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PMID:[The latent dysfunction of Epstein-Barr virus (EBV)-specific cellular immunity in asymptomatic human immunodeficiency virus (HIV) carriers]. 166 17

We present a patient with haemophilia A showing human immunodeficiency virus type 1 (HIV-1) infection and factor VIII inhibitor in whom a novel T-cell subpopulation, double-negative (CD4-CD8-) T cells bearing T-cell receptor (TCR)-alpha beta, proliferated polyclonally in the peripheral blood. An interleukin-2-dependent T-cell line with a CD4-CD8-TCR-alpha beta+ phenotype was established from the peripheral blood lymphocytes of the patient, and its biological functions were studied. It was found that the CD4-CD8-TCR-alpha beta+ T cells possessed both HLA-unrestricted cytotoxicity and helper function for immunoglobulin production by B cells. In addition, these T cells were found to produce interferon-gamma and interleukin-2 following activation via CD3-TCR complexes. These data demonstrating the multifunction of these newly defined CD4-CD8-TCR-alpha beta+ T cells thus suggest that these cells play an important role in protection against HIV infection. The mechanism of production of factor VIII inhibitor in the present case is also discussed focusing on the CD4-CD8-TCR-alpha beta+ T cells.
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PMID:Proliferation of double-negative (CD4-CD8-) T cells bearing T-cell receptor-alpha beta in a haemophiliac with human immunodeficiency virus type 1 infection and factor VIII inhibitor: functional properties of double-negative T-cell receptor-alpha beta+ T cells. 166 Nov 24

In 34 hearts, obtained at autopsy in consecutive AIDS cases, leukocytic phenotype and presence of viral antigens were investigated in paraffin-embedded (34 cases) and frozen myocardial sections (10 cases) by different monoclonal antibodies. The total frequency of focal lymphocytic infiltrates with and without myocell necrosis was 26.4 and 32.3%, respectively. In six control cases (HIV-negative i.v. drug abusers dying from acute fulminating hepatitis), these infiltrates were absent. In AIDS patients, the number of infiltrative foci per section, their wall distribution (subendocardial, middle layer, subepicardial), number of leukocytes per focus, and cell phenotype (prevalence of CD8+ suppressor/cytotoxic T-lymphocytes with CD4/CD8 ratio of 0.6 +/- 0.09 SE, absence of B-cells and granulocytes) were similar in cases with and without myocell necrosis. Significant differences were not observed between homosexual and i.v. drug abuser patients. In inflammatory foci associated with myocell necrosis CD45+/CD68+ monocytes prevailed, as a possible manifestation of nonspecific reparative process. In addition, in both AIDS patients and HIV-negative drug abusers, a population of CD68+ dendritic monocytes (histiocytes) characterized by a restricted CD45 expression (PanLeu-/9.4+) was found dispersed in the interstitium, with a significant higher frequency in the subendocardial layer. Histologic evidences of myocardial virus infections were not observed. Cytomegalovirus (CMV) antigens, however, were found in frozen sections of five of the six cases with lymphocytic infiltrates, supporting the view that this virus can be one of the possible causes of myocarditis in AIDS. Moreover, in two of these CMV-positive cases, a concomitant expression of HIV1 antigens in isolated intramyocardial leukocytes was also observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phenotype of intramyocardial leukocytic infiltrates in acquired immunodeficiency syndrome (AIDS): a postmortem immunohistochemical study in 34 consecutive cases. 166 94

A case is described of an HIV+ man who was successfully treated for Hodgkin's lymphoma, but who later developed non-Hodgkin's lymphoma 3 years later when his immune system became suppressed. The patient was 22 years old when he presented with fever, asthenia, weight loss, and cervical lymphadenopathy. With Hodgkin's lymphoma he also had positive serology for HIV and hepatitis B. He was treated with alternate courses of MOPP and ABVD chemotherapy. In 1990 he again appeared with high fever, progressive cervical, axillary and inguinal lymphadenopathy, with hilar and mediastinal lymph node enlargement on x-ray. CD4 lymphocytes were 577/cubic mm, and the CD4/CD8 ratio was 0.57 (normal 1.8). His cervical lymph node biopsy was classified as non-B non-T large-cell anaplastic lymphoma which was EBV-positive. A Western Blot was positive for small amounts of p24 and p18 antigens. The man was treated with MACOP-B chemotherapy, with some results, but died of sepsis 6 weeks later. The relationships between Hodgkins and non-Hodgkin's lymphoma, the timing of the neoplasm in the course of HIV infection, and the possible re-activation of hepatitis virus were discussed.
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PMID:Non-Hodgkin's lymphoma after prolonged remission of Hodgkin's disease in an HIV-infected patient. 166 42

Reduced CD4(+)-T-helper-lymphocyte- and increased CD8(+)-T-suppressor-lymphocyte-subsets were found in peripheral blood of 47 FIV-seropositive cats with naturally acquired FIV-infection. The CD4+/CD8+ ratio was decreased, too. Variance analysis of data included the variables reaction in FIV-test, age group, and race. Similarities with HIV-infection were discussed.
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PMID:[T-helper and T-suppressor lymphocyte subpopulations in the peripheral blood of spontaneously FIV-positive cats]. 166 2

In this paper is reported the first case of acquired immunodeficiency syndrome (AIDS) in the Chinese continent. In the initial stage, the patient (male) experienced fever, malaise and headache in April, 1990, and then developed repeated pulmonary infection and insidious progressive subacute encephalitis. The diagnosis of AIDS was confirmed by serological test for positive HIV antibody by enzyme linked immunosorbent assays(ELISA), immunofluorescence assays (IFA) and Western blot test(WB), significant reducing of CD4 lymphocyte, reverse of CD4/CD8 ratio and isolation of HIV-1 from peripheral blood in August, 1990. The patient died on September 2nd, 1990. In autopsy, there were generalized atrophy of lymph tissues, lymphocytic depletion, diffusive inflammation and necroses of the cerebral and cerebella parenchyma caused by toxoplasma, multifocal Kaposi's sarcoma of the stomach, and small intestine and bronchopneumonia.
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PMID:[First reported case of AIDS in China]. 166 68

T lymphocyte subsets were determined on blood samples from 16 HIV-seropositive patients with manifest AIDS (CDC IV), 24 HIV-seropositive patients with lymphadenopathy syndrome (LAS, CDC III), 16 HIV-seropositive clinical healthy persons (CDC II) and 11 HIV-seronegative homosexuals as control group. Absolute numbers of T-cells (CD6+), T-helper/inducer-cells (CD4+) and T-suppressor/cytotoxic-cells (CD8+), obtained by immunofluorescence staining were compared with the absolute amount of subset specific surface molecules, obtained by a T-cell-ELISA. With both, indirect immunofluorescence technique and ELISA technique a highly significant decrease of the absolute numbers of CD4+ cells and the absolute amount of CD4 surface molecules, respectively, was found in asymptomatic HIV-infection, LAS and in manifest AIDS. In all HIV-seropositive groups the relative decrease of CD4 surface molecules was significantly greater than the decline of CD4+ cells. This phenomenon however was not seen in HIV-seronegative homosexuals. The absolute number of CD6+ cells and the amount of CD6 surface molecules were found significantly lowered in AIDS compared to HIV-seronegative homosexuals. No significant changes were found for CD8+ cell numbers and CD8 surface molecule in the progression of the HIV-infection.
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PMID:Quantitative analysis of CD6, CD4 and CD8 cell surface molecules compared to the absolute numbers of CD6+, CD4+ and CD8+ T-cells in peripheral blood in patients with HIV-infection. 166 51

600 children born to HIV-infected mothers by June 15, 1990, in ten European centres were followed to study the natural history of HIV infection and the vertical transmission rate. They were seen at birth, every 3 months up to 18 months of age, and every 6 months thereafter. At last follow-up, 64 children were judged to be HIV infected and 343 had lost antibody and were presumed uninfected. The initial clinical feature in infected children was usually a combination of persistent lymphadenopathy, splenomegaly, and hepatomegaly, though 30% of children presented with AIDS, or with oral candidosis followed rapidly by AIDS. An estimated 83% of infected children show laboratory or clinical features of HIV infection by 6 months of age. By 12 months, 26% have AIDS and 17% die of HIV-related disease. Subsequently, the disease progresses more slowly and most children remain stable or even improve during the second year. The vertical transmission rate, based on results in 372 children born at least 18 months before the analysis, was 12.9% (95% Cl 9.5-16.3%). Virus has been repeatedly isolated in an additional small proportion of children (2.5%, 95% Cl 0.7-6.3%) who lost maternal antibody and have remained clinically and immunologically normal. Without a definitive virological diagnosis, the monitoring of immunoglobulins, CD4/CD8 ratio, and clinical signs could identify HIV infection in 48% of infected children by 6 months, with a specificity of more than 99%.
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PMID:Children born to women with HIV-1 infection: natural history and risk of transmission. European Collaborative Study. 167 Nov 9


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